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l asparaginase/seizures
Врската е зачувана во таблата со исечоци
Страница 1 од 43 резултати
A Young Boy with L-asparaginase-Induced Seizure.
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L-Asparaginase is a critical component in the treatment of acute lymphoblastic leukemia in children. It is known to cause coagulation abnormalities, thrombosis and hemorrhage in the central nervous system in addition to vasculitis and hypersensitivity reactions. This syndrome generally occurs after
L-asparaginase-provoked seizures as singular expression of central nervous toxicity.
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Patients treated with L-asparaginase may present with hemorrhagic and thrombotic cerebrovascular events. This syndrome generally occurs after a few weeks of therapy and may occur after L-asparaginase therapy is completed. Complications appear to result from depletion of plasma proteins involved in
Intracranial hemorrhage and focal seizures secondary to use of L-asparaginase during induction therapy of acute lymphocytic leukemia.
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L-Asparaginase is commonly used for induction therapy of acute lymphocytic leukemia of childhood. Severe clinical bleeding secondary to clotting dysfunction has not been previously reported. We observed intracranial hemorrhagic infarcts with focal seizures and hemiparesis associated with clotting
Epileptic seizures after octreotide administration in a 6.5-year-old female with ALL and L-asparaginase associated pancreatitis: a possible drug interaction.
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BACKGROUND
Octreotide is a synthetic somatostatin analogue which has been suggested for use in the management of acute pancreatitis, though its safety and effectiveness in the pediatric setting has not been extensively studied.
METHODS
we present a rare case of a 6.5-year-old female with acute
A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia.
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L-Asparaginase therapy for childhood acute lymphoblastic leukemia causes deficiencies of plasma hemostatic proteins, especially antithrombin, plasminogen, and fibrinogen. Severe thromboses and hemorrhages occurred in 18 children receiving vincristine, prednisone, and asparaginase therapy for ALL.
L-asparaginase-induced posterior reversible encephalopathy syndrome during acute lymphoblastic leukemia treatment in children.
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L-asparaginase is a critical component in the treatment of acute lymphoblastic leukemia in children. It is known to cause coagulation abnormalities, thrombosis and hemorrhage in the central nervous system in addition to vasculitis and hypersensitivity reactions. The purpose of this article is to
[Fulminant hepatitis possibly caused by L-asparaginase during induction chemotherapy in a patient with acute lymphoblastic leukemia].
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We report a 44-year-old man with acute lymphoblastic leukemia (ALL) presenting with fever and lymphadenopathy. Induction chemotherapy was initialed according to the JALSG ALL202 protocol, and L-asparaginase (L-asp) was given on days 20, 22, and 24 of therapy. Abrupt elevations of liver transaminase
Prognosis and treatment of seizures in children with acute lymphoblastic leukemia.
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We reviewed the records of 127 consecutive pediatric patients with acute lymphoblastic leukemia (ALL) to determine the incidence, timing, etiologies, and recurrence rate of seizures in this population. Patients with ALL and seizures were identified retrospectively by review of the records of all
[Reversible posterior leukoencephalopathy syndrome probably caused by L-asparaginase].
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A 46-year-old male with refractory biphenotypic acute leukemia was treated with doxorubicin (days 1-3, 15-17), vincristine (days 1, 8, 15, 22), prednisolone (days 1-28), and L-asparaginase (L-ASP: days 15-28) as reinduction therapy. Physical examination revealed normotensive state and normal
Sagittal sinus thrombosis due to L-asparaginase.
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Cerebral Sinovenous Thrombosis (CSVT) is a serious complication of L-asparaginase chemotherapy for leukemia in children. Clinical features of headache, altered consciousness, focal neurological deficit, and seizures developing during or immediately after treatment with L-asparaginase should alert
Recurrent cerebrovascular accident with L-asparaginase rechallenge.
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We report a 15-year-old boy diagnosed with acute lymphoblastic leukemia (ALL) in 1983. Induction therapy included L-asparaginase. After the second dose of L-asparaginase, he had a left sided focal seizure and computed tomography (CT) scan of the head showed a right frontal infarct. No further
Neurosurgical management of L-asparaginase induced haemorrhagic stroke.
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The authors describe a case of L-asparaginase induced intracranial thrombosis and subsequent haemorrhage in a newly diagnosed 30-year-old man with acute lymphoblastic leukaemia who was successfully managed by surgical intervention. At presentation, he had a Glasgow Coma Score of 7/15, was aphasic
Parathyroid necrosis and hypocalcemic tetany induced in rabbits by L-asparaginase.
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Fifty percent of New Zealand white rabbits became profoundly weak, had generalized seizures and died between 22 and 47 hours after an intravenous injection of 1000 IU/kg of L-asparaginase. The biochemical correlate of this syndrome is severe hypocalcemia associated with marked, single cell,
L-asparaginase-induced reversible posterior leukoencephalopathy syndrome in a child with acute lymphoblastic leukemia.
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Reversible posterior leukoencephalopathy syndrome (RPLS) is being increasingly described with various etiologies even in the absence of hypertension. We present an 11-year-old patient with acute lymphoblastic leukemia who presented with seizures while on treatment with L-asparaginase. MRI showed
Hyperglycemia, ketoacidosis and other complications of L-asparaginase in children with acute lymphoblastic leukemia.
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We show Escherichia coli derived L-asparaginase complications observed in 14 of 136 acute lymphoblastic leukemia patients during remission induction therapy according to St. Jude Children's Hospital Total XI Protocol. We observed hyperglycemia in six patients; two of them had accompanying
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